Table 1.
Characteristics | European Americans* (n = 762) | African Americans (n = 595) | P |
---|---|---|---|
Age, y (mean ± SD) | 64.1 ± 15.2 | 57.0 ± 15.7 | <.001 |
Height, inches (mean ± SD) | 67.9 ± 4.0 | 67.4 ± 6.6 | .08 |
Weight, pounds (mean ± SD) | 192.8 ± 50.1 | 200.6 ± 51.1 | .005 |
BSA, m2 (mean ± SD) | 2.0 ± 0.3 | 2.0 ± 0.3 | .17 |
Female | 324 (42.5) | 336 (56.5) | <.001 |
Current smoker | 72 (9.5) | 97 (16.3) | <.001 |
Indication for warfarin therapy | |||
Venous thromboembolism | 265 (34.8) | 314 (52.8) | <.001 |
Stroke/transient ischemic attack | 33 (4.3) | 41 (6.9) | .04 |
Atrial fibrillation | 403 (52.9) | 170 (28.6) | <.001 |
Myocardial infarction | 12 (1.6) | 11 (1.9) | .69 |
Peripheral arterial disease | 7 (0.9) | 7 (1.2) | .64 |
Other | 42 (5.5) | 51 (8.6) | .03 |
Comorbid conditions | |||
Hypertension | 464 (61.6) | 425 (72.2) | <.001 |
Hyperlipidemia | 410 (54.5) | 238 (40.4) | <.001 |
Diabetes mellitus | 202 (26.8) | 224 (38.0) | <.001 |
CKD† | |||
eGFR ≥60 mL/min/1.73 m2 | 460 (60.5) | 378 (63.7) | |
eGFR ≥30-59 mL/min/1.73 m2 | 256 (33.7) | 134 (22.6) | <.001 |
eGFR <30 mL/min/1.73 m2 | 44 (5.8) | 81 (13.7) | |
Concurrent medications | |||
Statins‡ | 444 (58.3) | 291 (49.4) | .001 |
Antiplatelets§ | 472 (61.9) | 322 (54.7) | .007 |
Amiodarone | 99 (12.9) | 42 (7.1) | <.001 |
Percentage of patients possessing ≥1 minor allele|| | |||
CYP2C9*2 | 25.6 | 4.9 | <.001 |
CYP2C9*3 | 12.6 | 2.3 | <.001 |
CYP2C9 *5, *6, *11 | 0.0 | 3.4 | <.001 |
CYP2C9 *8 | 1.1 | 13.9 | <.001 |
VKORC1 | 60.2 | 18.5 | <.001 |
CYP4F2 | 51.9 | 16.4 | <.001 |
rs12777823 | 30.6 | 42.1 | <.001 |
FPGS | 0.0 | 40.4 | — |
EPHX1 | 52.7 | 29.3 | <.001 |
GGCX | 55.6 | 86.9 | <.001 |
CALU | 35.6 | 13.2 | <.001 |
Data are presented as n (%) of participants unless otherwise indicated.
eGFR, estimated glomerular filtration rate; SD, standard deviation.
Asians (n = 4; 0.3%) and Hispanics (n = 5; 0.4%) were combined with the European Americans group as non–African Americans were combined into 1 race group in COAG.
All eGFRs are based on National Kidney Foundation staging using the Modification of Diet in Renal Disease study equation. Patients were categorized into 3 categories: GFR ≥60 (no CKD or mild CKD stage 1 and 2), GFR = 30 to 59 (moderate CKD; stage 3), and GFR <30 (severe CKD; stage 4 and 5).
Statins included any of the 3-hydroxy-3-methyl-glutaryl–coenzyme A reductase inhibitors.
Antiplatelet agents included aspirin, clopidogrel, and dipyridamole as monotherapy or dual therapy.
CYP2C9*2, CYP2C9*3, CYP4F2, and VKORC1 were included as additive: 0 if no variants, 1 if heterozygous, and 2 if homozygous for the variant allele. CYP2C9*5, *6, and *11 together and CYP2C9*8, rs12777823, FPGS (rs7856096), EPHX1 (rs1051740), GGCX (rs699664), and CALU (rs2290228) were categorized as 0 if no variants and 1 if heterozygous or homozygous for the variant allele. Genotyping was not complete for some patients at the time of analysis, and therefore, genotype information is not available in 86 patients for CYP2C9, 828 patients for CYP2C9*8 (rs7900194 “A” allele), 57 patients for VKORC1 (rs9923231 “T” allele), 117 patients for CYP4F2 (rs2108622; A allele), and 118 patients for rs12777823 (A allele). Analysis of the influence of FPGS (rs7856096; “G” allele), EPHX1 (rs1051740; G allele), GGCX (rs699664; T allele), and CALU (rs2290228; A allele) was restricted to 290 patients.